What is The Pathophysiology of OCD?

When trying to better understand obsessive-compulsive disorder (OCD), you must consider its pathophysiology. Objective analysis and evaluation (critical thinking) and an ability to accurately assess an OCD sufferer’s mental health needs, and determine the right intervention or treatment plan for him or her (clinical reasoning).

These two elements – critical thinking and clinical reasoning can lead to the correct clinical diagnoses and practices. Also, to understand the pathophysiology of OCD, you must take into account that it will likely involve other fields of study, such as biochemistry, pharmacology, psychology, etc. The truth is you cannot battle OCD, if you are unsure of its possible origins or if you do not fully understand the ins and outs of the condition.

There have been various psychological and biological theories surmised to help mental health professionals and the general population better understand the pathophysiology of OCD. However, the consensus is that hormones/neurotransmitters, like serotonin, play an important role in the pathophysiology.

If you would like to learn more about pathophysiology and how it is connected to OCD, keep reading. This article may even better understand what triggered your OCD symptoms.

First, What is OCD?

OCD, also clinically known as obsessive-compulsive disorder, is a fairly common, chronic anxiety condition characterized by non-stop, intrusive, violent, sexual, or upsetting thoughts, urges, fears, doubts, worries, mental images, and/or negative emotions (obsessions) and/or repetitive and ritualistic behaviors (compulsions). Some people only have obsessions (pure O). Some people only have compulsions (rituals and routines).

The majority of OCD sufferers, on the other hand, struggle with both obsessions and compulsions. OCD is usually diagnosed by a trained and experienced OCD therapist through psychological assessments, self-reports of symptoms, and therapist/client observations. OCD may not appear to be emotionally distressing, although it is. OCD is powerful, time-consuming, and energy-zapping. It is also a “destroyer” demolishing everything in its sight. Nothing or no one is safe with this condition – it can damage or destroy your relationships, self-esteem and self-confidence, and ability to make friends with people in your peer group.

The good news is that it can be treated with psychotherapy like cognitive-behavioral disorder (CBT), exposure-response and prevention (ERP) therapy, and/or acceptance and commitment therapy (ACT), medication, like selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants, and/or antipsychotics.

Natural remedies, alternative/holistic treatments, and self-help tools, like CBD, mindfulness meditation, OCD support groups, forums, books, and podcasts, hypnotherapy/hypnosis, healthy coping skills and strategies, a healthy diet filled with nutritious vitamins and minerals (i.e., magnesium), quality sleep, plenty of exercises, and Impulse Therapy, an online OCD treatment program. Medication(s) are usually prescribed when therapy is unsuccessful. This is called treatment-resistant OCD.

What is Pathophysiology?

According to researchers, pathophysiology is the study of the atypical or uncommon physiological processes linked to an injury or condition. Pathophysiology studies the etiology or “causes” (i.e., congenital and genetic causes, and acquired diseases) of mental and physical health conditions and diseases.

Pathophysiology also studies the signs and symptoms of various conditions and diseases (i.e., the objective and subjective “evidence” of conditions and diseases. These signs are considered objective evidence, such as behaviors that one can see (i.e., rituals or routines). In contrast, subjective evidence tends to be “unclear” like intrusive thoughts, urges, mental images, worries, doubts, fears, and other mental OCD obsessions. Regardless of whether the “evidence” is objective or subjective, both types require more studies.

Pathophysiology also involves investigating the signs and symptoms of conditions and diseases to determine an accurate diagnosis. Investigations may include observing a person’s behavior, listening to him or her recount his or her signs and symptoms, reviewing journal entries, and/or using psychological assessments to ensure he or she is being diagnosed with the right condition – i.e., OCD. Understand, however, that some conditions, like OCD, cannot be diagnosed with lab tests or x-rays. Thus, the purpose of this investigation or study is to unearth the true cause of the signs and symptoms to formally diagnose the condition or disease.

Treatment is another important part of pathophysiology. For instance, an OCD therapist is responsible for administering the treatment to his or her clients or patients. As a result, your OCD therapist needs to have sound knowledge of the pathophysiology of OCD.

Pathophysiology also allows you to determine the prognosis. For instance, a client’s or patient’s chance of survival or recovery (i.e., OCD recovery). A therapist may determine that the client or patient has a good chance of a full or partial survival or recovery, or no survival or recovery.

How Does Pathophysiology Apply to OCD?

Research suggests that the pathophysiology of OCD lies in a wide range of brain regions. As a result, several theories have been formulated on how these regions apply to and affect OCD.

Listed below are pathophysiology OCD theories:

The Serotonin Theory

Studies suggest that serotonin has almost always had a role in the development and progression of OCD. During the 1960s, researchers found that clomipramine, a tricyclic antidepressant with strong serotonin reuptake-blocking properties, produce anti-obsession effects in the mind. Moreover, studies indicate that clomipramine and other selective serotonin reuptake inhibitors (SSRIs), like Paxil, Prozac, Zoloft, etc., also produce anti-obsession effects in the mind.

According to researchers, serotonin may play an important role in the pathogenesis of OCD. Thus, most studies on OCD and serotonin found that OCD sufferers have an imbalance in serotonin, specifically a serotonin deficiency or low levels of serotonin in the brain. This serotonin imbalance can trigger or worsen OCD symptoms, especially OCD obsessions. 

OCD sufferers also appear to have a hyperactive serotonin receptor neurotransmission system, due to hypersensitive postsynaptic receptors or a hypoactive presynaptic receptor, which is responsible for “self-regulation.”

This may explain the worsening OCD symptoms after acute serotonin receptor stimulation, and the improvement of OCD symptoms after the chronic administration of proserotonergic compounds. In other words, the chronic administration of clomipramine or SSRIs can trigger serotonin receptors, causing a release of serotonin in the orbitofrontal cortex. Study results also indicate that serotonin (from SSRIs) can stay in an OCD sufferer’s system for 6 to 8 weeks, which is longer than most other antidepressants – even at high dosages).

Keep in mind, however, that some OCD sufferers may not respond to clomipramine or SSRIs – with almost 30% of these individuals not benefiting from the extra serotonin at all. Researchers believe that biological heterogeneity of the OCD phenotype may influence the mind’s and body’s response to the extra serotonin.

Dorsolateral Prefrontal Cortex (DLPC) Theory

The dorsolateral prefrontal cortex (DLPC) is essential for “normal” cognitive functions in people. Studies suggest that DLPC is linked to one’s “working memory.” DLPC’s job is to help you adapt to changes in your environment. It also supports sound judgment and helps you focus on specific stimuli. DLPC lesions can disrupt an OCD sufferer’s ability to accurately process temporal lobe information/data, and prevent him or her from successfully performing goal-directed tasks and behaviors.

The theory is that people, who struggle with mental health conditions, like depression and OCD, experience a decline in the DLPC region. This decline may account for how hard it is for an OCD sufferer to stop engaging in compulsive behaviors.

Anterior Cingulate Cortex (ACC) Theory

According to neuroimaging studies, the anterior cingulate cortex (ACC) (i.e., dorsal or cognitive region and ventral or affective region) plays an important role in a variety of cognitive functions, such as focus and concentration, self-awareness, motivation, reward, error detection, “working memory,” problem solving, and action planning. The theory is that continuous, frequent, or excessive activation of ACC can trigger mood disorders, phobias, and/or OCD in some people. There is also a link between the error detection process and obsessions and compulsions.

Thalamus Theory

The thalamus aids in emotional expression through the anterior nucleus of the thalamus (AN), which is connected to the mammillary bodies (MB). The thalamus sends estimations or a prognosis to the ACC. The ventral anterior nucleus of the thalamus plays an important role in cognitive functions that involve focus, concentration, attention, and “working memory,” stemming from its link with the DLPC.

Some parts of the medial dorsal nucleus of the thalamus appear to play a role in emotional processes and cognitive processes. Thalamic disruptions have been linked to executive function deficits, such as planning, goal-directed behaviors, focus, concentration, attention, and “working memory.” The theory is that a disruption in thalamus function can trigger or exacerbate OCD thoughts and behaviors.

Orbitofrontal Cortex (OFC) Theory

The orbitofrontal cortex (OFC) is a massive brain region that involves the rostral and ventromedial areas. This part of the brain receives multimodal data from the temporal association cortex, amygdala, hypothalamus, and the limbic part of the basal ganglia. Together, these brain regions are responsible for emotional processing and regulation. The OFC is located in the prefrontal temporal lobe area and appears to play an important role in a person’s internal reward system – i.e., incentives, bonuses, rewards, and in conditions. It also appears to arise when a person has to make quick changes in behavior to adapt to changes in his or her environment.

Thus, researchers have found that OFC is needed for making reward-based decisions. People with damage to their orbitofrontal cortexes typically have a hard time making sound decisions. These individuals also tend to take unnecessary risks, regardless of the consequences. OFC neurons (nerves) tend to become especially active when a person is put in a situation, where he or she receives a reward or expects to receive one. Studies suggest that OFC neurons may be connected in the link between rewards and facial expressions. For instance, positive rewards can typically elicit smiles, smirks, winks, and/or laughter.

OFC also appears to play an important role in the motivational element of making decisions. Moreover, the left inferior parietal cortex and parietooccipital junction appear to be heavily involved in visual-based cognitive tasks. The theory is that low levels of activity in these brain regions can cause spatial and visual memory deficits commonly found in OCD sufferers. Therefore, the consensus is that compulsions and aggression, commonly found in people with OCD are likely due to a depletion of serotonin in the brain.

Amygdala Theory

The amygdala comprises several nuclei (central parts of the nucleus), such as the lateral nucleus, basolateral nucleus, and central nucleus. Studies suggest that the amygdala is not only involved in negative emotions, like anxiety, fear, doubt, worry, etc., but also incentives and positive emotions, like happiness, relief, excitement, etc. Thus, researchers have found that the amygdala plays an essential role in emotional expression, and motivation likely through its association with the OFC, ACC, and ventral striatum. The theory is that an imbalance, disruption, or dysfunction in the amygdala can trigger stress and anxiety, commonly linked to OCD obsessions.

Mesocorticolimbic Dopaminergic System & Dopamine Theory 

The mesocorticolimbic dopaminergic system (a pathway in the brain that carries dopamine from one brain region to another). Dopamine, a hormone/neurotransmitter, influences a person’s reward and pleasure sensations. Dopamine also plays a role in organizational processes and the regulation of goal-directed behaviors. The mesocorticolimbic dopaminergic system also contributes to a person’s attention, motivation, and emotions. 

Dopamine is usually associated with serotonin, while the mesocorticolimbic dopaminergic system is linked to serotonin-producing neurons, which are located in the brainstem raphe nuclei. Serotonin, in general, is responsible for behavior. And, while balanced levels of serotonin are associated with positive behaviors, low levels of serotonin (serotonin deficiency) are associated with increased hyper-exploration, increased motor activities, aggression, and sexual behaviors. The theory is that compulsions, along with sexual and/or aggressive behaviors in people with OCD people likely stem from a serotonin deficiency.

Striatum Theory

The striatum involves two types of information-processing components – striasomes and matrisomes. Striasomes receive data from the limbic structures (i.e., amygdala, OFC, and ACC), and then transfer that data to the dopaminergic neurons of the substantia nigra. Striasomes are believed to be responsible for regulating and modifying the emotional aspects of cortical information. 

Matrisomes, on the other hand, receive data from the lateral parts of the premotor and prefrontal cortices. Matrisomes are believed to be responsible or at least involved in planning and anticipatory behaviors. Striasomes and matrisomes are involved in processing important information, such as the detection of unanticipated events, or the context of events or behaviors. 

Researchers believe that the limbic region of the ventral striatum may be involved in reward-driven learning processes. Conversely, the dorsal striatum appears to be involved in the learning of semiconscious behavioral rituals and routines. The theory is that disrupted striatum “readiness” and “release” functions may lead to OCD symptoms, along with emotionally modifying information, and the context of events and behaviors.

To Sum It Up…

Brain scans reveal that OCD sufferers have different brain activities (neurodivergence) than other people (neurotypical). Moreover, studies indicate that there is a “miscommunication” or “disruption” between the orbital frontal cortex, the caudate nucleus, and the thalamus, which can trigger or worsen OCD symptoms. More specifically, when the caudate nucleus does not function properly, it triggers a hyperactive thalamus that continuously sends “worry” messages back and forth between the OFC and itself. The OFC’s response? An overload of stress and anxiety.

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